Adherens junctions have an important role in the control of vascular permeability. These structures are located at cell-to-cell contacts, mediate cell adhesion and transfer intracellular signals. Adhesion is mediated by cadherins, which interact homophilically in trans and form lateral interactions in cis. VE-cadherin (also known as CDH5 and CD144) is the major component of endothelial adherens junctions and is specific to endothelial cells. Endothelial cells from different types of vessels, such as lymphatic vessels, arteries and veins, show differences in junction composition and organization. Vascular permeability is increased by modifications in the expression and function of adherens junction components. In some cases these defects might be cause of pathology. In this Cell Science at a Glance article, we present the example of the so-called cerebral cavernous malformation (CCM), where adherens junctions are dismantled in the vessels contributing to brain microcirculation. This causes the ...
The structure and physiology of the endothelial cells that line the mammalian vasculature are greatly influenced by the shear stresses that are continuously imposed on them by blood flow. The most obvious structural responses of endothelium to shear stress are changes in cell shape and orientation; in areas of low or inconsistent shear stress in vivo, or when cells are maintained in static culture, endothelial cells assume a cuboidal, cobblestone morphology, whereas they elongate and align in the direction of flow when shear stress is moderate or high.1 2 These morphological changes are adaptive in that they reduce the spatial fluctuations in shear stress and the maximum shears to which the cells are exposed.3 Shape change of cells within monolayers probably necessitate changes in the interaction of individual cells with their neighbors at cell-cell junctions; however, changes in endothelial cell-cell contacts during responses to altered shear stress have not been examined. Endothelial cells ...
The intercellular Adherens Junctions (AJs) are specialized sub-apical structures that function as principle mediators of cell-cell adhesion. Their disassembly correlates with a loss of cell-cell contact and an acquisition of migratory potential. The Adherens Junctions have a crucial role both as sensors of extracellular stimuli and in regulating the dynamics of epithelial cell sheets or with neighboring cells. Cadherins, the Type-I transmembrane proteins of the Adherens Junctions, are principally responsible for homotypic cell-cell adhesion. E-Cadherin, which is present primarily in epithelia, is the best-characterized Cadherin and represents the prototype of classical Cadherins. The extracellular domain of E-Cadherin binds to Ca2+ (Calcium) and forms complexes with the extracellular domains of E-Cadherin molecules on neighboring cells. The cytoplasmic domain of E-Cadherin associates with cytosolic proteins called Catenins (Alpha, Beta and p120), which in turn provide anchorage to the Actin ...
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Formation of blood vessel networks by sprouting angiogenesis is critical for tissue growth, homeostasis and regeneration. How endothelial cells arise in adequate numbers and arrange suitably to shape functional vascular networks is poorly understood. Here we show that YAP/TAZ promote stretch-induced proliferation and rearrangements of endothelial cells whilst preventing bleeding in developing vessels. Mechanistically, YAP/TAZ increase the turnover of VE-Cadherin and the formation of junction associated intermediate lamellipodia, promoting cell migration whilst maintaining barrier function. This is achieved in part by lowering BMP signalling. Consequently, the loss of YAP/TAZ in the mouse leads to stunted sprouting with local aggregation as well as scarcity of endothelial cells, branching irregularities and junction defects. Forced nuclear activity of TAZ instead drives hypersprouting and vascular hyperplasia. We propose a new model in which YAP/TAZ integrate mechanical signals with BMP signaling ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
The ability of cells to assemble into tissues, organs, and animals depends on cell-cell adhesion (for reviews see Yap et al., 1997; Tepass et al., 2001). The central mediators of cell adhesion are proteins of the cadherin-catenin complex, which localize to adherens junctions (AJs),* adhesive junctions near the apical end of the lateral cell interface of epithelial cells. Transmembrane cadherins mediate homophilic adhesion, whereas catenins anchor cadherins to actin at adhesion sites. β-catenin (β-cat) and its Drosophila ortholog Armadillo (Arm) bind directly to both the distal region of the cadherin cytoplasmic tail and to α-catenin (α-cat). α-Cat interacts with actin both directly and indirectly. Cadherins, β-cat, and α-cat play essential roles in adhesion-genetic experiments in animals and in cell culture reveal that adhesion is abolished in their absence. Consistent with this, the cadherin tail is important for strong cell-cell adhesion, at least in some cells.. However, ...
Cadherins mediate homophilic, Ca2+-dependent cellular adhesion at adherens junctions. Experiments in MDCK cells, which provide a model for cadherins at adherens junctions, demonstrated the formation of cadherin-NPRAP-ABP complexes dependent on the expression of NPRAP and the integrity of the NPRAP-ABP interaction, and the formation of NPRAP-ABP-GluR2 complexes dependent on expression of ABP. This suggests that the proposed cadherin-NPRAP-ABP-GluR2 complexes can indeed form in cells. Two dominant-negative mutants of NPRAP were assayed for their effects on GluR2. One mutant does not interact with ABP, GRIP, or PSD-95, and the second binds these scaffolding proteins but does not bind to cadherins. Both mutants reduced GluR2 surface levels. This suggests that cadherin-NPRAP-ABP-GluR2 complexes contribute to the surface stabilization of GluR2. In neurons, adherens junction structures containing cadherins are found at synapses (Takeichi and Abe, 2005). This suggests that the AMPARs that are anchored ...
Proteins and other substances can cross the endothelial layer that lines a blood vessel via two routes. Caveolin-1 is essential for both, Siddiqui et al. show.. Researchers already knew that caveolin-1 was necessary for transcellular protein trafficking, in which macromolecules such as albumin enter an endothelial cell from the bloodstream and exit on the tissue side. Caveolae swallow these molecular travelers and bundle them into vesicles that wend through the cell. In an alternative pathway, known as the paracellular route, molecules slip between the cells of the endothelial layer, passing through the adherens junctions that fasten adjacent cells together. Previous work showed that adherens junctions become permeable in mice lacking caveolin-1, suggesting that the protein helps seal the junctions.. Siddiqui et al. dissected the molecular chain of events that connects caveolin-1 to adherens junction integrity. Loss of caveolin-1 activated the enzyme eNOS, which spawns nitric oxide (NO) that ...
Intercellular junctions play a pivotal role in tissue development and function and also in tumorigenesis. In epithelial cells, decrease or loss of E-cadherin, the hallmark molecule of adherens junctions (AJs), and increase of N-cadherin are widely thought to promote carcinoma progression and metastasis. In this paper, we show that this "cadherin switch" hypothesis does not hold for diverse endoderm-derived cells and cells of tumors derived from them. We show that the cadherins in a major portion of AJs in these cells can be chemically cross-linked in E-N heterodimers. We also show that cells possessing E-N heterodimer AJs can form semistable hemihomotypic AJs with purely N-cadherin-based AJs of mesenchymally derived cells, including stroma cells. We conclude that these heterodimers are the major AJ constituents of several endoderm-derived tissues and tumors and that the prevailing concept of antagonistic roles of these two cadherins in developmental and tumor biology has to be reconsidered. ...
TFEB Controls Vascular Development by Regulating the Proliferation of Endothelial Cells In endothelial cells, transcription factor EB (TFEB) depletion halted proliferation at the G1-S transition by inhibiting the cyclin-dependent kinase 4/retinoblastoma pathway. TFEB-deficient cells attempted to compensate for this limitation by increasing VEGFR2 levels at the plasma membrane via microRNA-mediated mechanisms and controlled membrane trafficking. [EMBO J] Full Article , Graphical Abstract SENCR Stabilizes Vascular Endothelial Cell Adherens Junctions through Interaction with CKAP4 Levels of SENCR RNA were shown to be elevated in several differentiated human endothelial cell (EC) lineages subjected to laminar shear stress. SENCR loss-of-function studies disclosed perturbations in EC membrane integrity resulting in increased EC permeability. [Proc Natl Acad Sci USA] Abstract Engineering an Environment for the Study of Fibrosis: A 3D Human Muscle Model with Endothelium Specificity and Endomysium The ...
Vascular adherens junctions are key components in the regulation of endothelial barrier permeability; as such, it has been proposed that they have the capacity to sense and respond to various mechanical forces that are present in their environment. Cadherins are the main cohesion proteins of adherens junctions, and epithelial cadherins are known to be force sensitive. However, in the endothelium the precise role of vascular endothelial (VE) cadherin in mechanotransduction is poorly understood. Here (p. 1341), Deborah Leckband and colleagues investigate the function of VE-cadherin in force sensation within pulmonary endothelial cells. Using magnetic twisting cytometry, the authors showed that VE-cadherin directly sensed mechanical force and transmitted the signal to the cytoskeleton, resulting in local F-actin and vinculin recruitment and inter-endothelial junction remodelling. The authors also report that force transduction through both VE-cadherin and (platelet endothelial-cell adhesion ...
When DArcy Wentworth Thompsons On Growth and Form was published 100 years ago, it raised the question of how biological forms arise during development and across evolution. In light of the advances in molecular and cellular biology since then, a succinct modern view of the question states: how do genes encode geometry? Our new special issue is packed with articles that use mathematical and physical approaches to gain insights into cell and tissue patterning, morphogenesis and dynamics, and that provide a physical framework to capture these processes operating across scales.. Read the Editorial by guest editors Thomas Lecuit and L. Mahadevan, as they provide a perspective on the influence of DArcy Thompsons work and an overview of the articles in this issue.. ...
Formins are a diverse class of actin regulators that influence filament dynamics and organization. Several formins have been identified at epithelial adherens junctions, but their functional impact remains incompletely understood. Here, we tested the hypothesis that formins might affect epithelial interactions through junctional contractility. We focused on mDia1, which was recruited to the zonula adherens (ZA) of established Caco-2 monolayers in response to E-cadherin and RhoA. mDia1 was necessary for contractility at the ZA, measured by assays that include a FRET-based sensor that reports molecular-level tension across αE-catenin. This reflected a role in reorganizing F-actin networks to form stable bundles that resisted myosin-induced stress. Finally, we found that the impact of mDia1 ramified beyond adherens junctions to stabilize tight junctions and maintain the epithelial permeability barrier. Therefore, control of tissue barrier function constitutes a pathway for cadherin-based ...
Involvement of nectin in the localization of IQGAP1 at the cell-cell adhesion sites through the actin cytoskeleton in Madin-Darby canine kidney cells. Katata, Tatsuo; Irie, Kenji; Fukuhara, Atsunori; Kawakatsu, Tomomi; Yamada, Akio; Shimizu, Kazuya; Takai, Yoshimi // Oncogene;4/10/2003, Vol. 22 Issue 14, p2097 IQGAP1, a putative downstream target of the Rho family small G proteins, Cdc42 and Rac, localizes at adherens junctions (AJs) in epithelial cells. It has been suggested that IQGAP1 localizes at AJs through its binding to ?-catenin, and negatively regulates the E-cadherin-mediated cell-cell... ...
Thrombospondin-1 (TSP) induces endothelial cell (EC) actin reorganization and focal adhesion disassembly and influences multiple EC functions. To determine whether TSP might regulate EC-EC interactions, we studied the effect of exogenous TSP on the movement of albumin across postconfluent EC monolayers. TSP increased transendothelial albumin flux in a dose-dependent manner at concentrations ≥1 μg/ml (2.2 nM). Increases in albumin flux were observed as early as 1 h after exposure to 30 μg/ml (71 nM) TSP. Inhibition of tyrosine kinases with herbimycin A or genistein protected against the TSP-induced barrier dysfunction by >80% and >50%, respectively. TSP-exposed monolayers exhibited actin reorganization and intercellular gap formation, whereas pretreatment with herbimycin A protected against this effect. Increased staining of phosphotyrosine-containing proteins was observed in plaque-like structures and at the intercellular boundaries of TSP-treated cells. In the presence of protein tyrosine ...
Background The dynamic regulation of cell-cell adhesions is crucial for developmental processes, including tissue formation, differentiation and motility. Adherens junctions are important components...
The role of cis interactions between cadherins is less established, with no clear consensus on precisely which domains are engaged in these interactions (as reviewed in [3]). Recent evidence however suggests that these interactions are not required to facilitate trans interactions [8], whereas trans interactions are required in order for cis interactions to occur [9]. Computational modeling has been carried out to determine how these interactions, both trans and cis, result in the formation of a stable junction [9]. These in silico experiments showed that cadherins freely floating in the plasma membrane are not able to successfully form trans dimers unless their diffusion is slowed down in some manner. The introduction of a diffusion trap permitted the formation of trans dimers, however without subsequent cis interactions these trans dimers were unable to coalesce to form an ordered structure. Though weak, cis interactions were nonetheless shown to be vital for junction formation. Moreover, the ...
When DArcy Wentworth Thompsons On Growth and Form was published 100 years ago, it raised the question of how biological forms arise during development and across evolution. In light of the advances in molecular and cellular biology since then, a succinct modern view of the question states: how do genes encode geometry? Our new special issue is packed with articles that use mathematical and physical approaches to gain insights into cell and tissue patterning, morphogenesis and dynamics, and that provide a physical framework to capture these processes operating across scales.. Read the Editorial by guest editors Thomas Lecuit and L. Mahadevan, as they provide a perspective on the influence of DArcy Thompsons work and an overview of the articles in this issue.. ...
has likely a key role in regulating recycling through the RAB11A-dependent perinuclear recycling compartment, and links the regulation of adherens junctions to recycling to allow dynamic modulation of intercellular adhesion ...
Group 5: Adherens Junctions Introduction: The introductions sentence structure is a bit difficult to understand. Whilst much of the content is there, it could be written a bit clearer. Also a bit of an overview on what will be discussed would be helpful for the reader. History: The history has too few enteries, however the layout makes it easy to read and understand. Structure: The structure is informative and the adjoining pictures are good, giving the reader an idea of their form on a molecular and what they actually look like through a microscope. Function: Whilst the section is clearer, it could be made even more accessible by the addition of subheadings for the main functions. Importance And Regulation: The link to the picture at the beginning of this section does look very detailed and important to your subject, however it may be better to either explain the link or upload the actual picture to the page. Also the extracellular regulator sentence would be more informative and professional ...
Complete information for AJAP1 gene (Protein Coding), Adherens Junctions Associated Protein 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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Dynamic regulation of cell-cell adhesion by the coordinated formation and dissolution of E-cadherin-based adherens junctions is crucial for tissue homeostasis. The actin-binding protein cortactin interacts with E-cadherin and enables F-actin accumulation at adherens junctions. Here, we were interested to study the broader functional interactions of cortactin in adhesion complexes. In line with literature, we demonstrate that cortactin binds to E-cadherin, and that a posttranslational modification of cortactin, RhoA-induced phosphorylation by protein kinase D1 (PKD1;also known as PRKD1) at S298, impairs adherens junction assembly and supports their dissolution. Two new S298-phosphorylation-dependent interactions were also identified, namely, that phosphorylation of cortactin decreases its interaction with beta-catenin and the actin-binding protein vinculin. In addition, binding of vinculin to beta-catenin, as well as linkage of vinculin to F-actin, are also significantly compromised upon ...
Looking for online definition of zona adherens in the Medical Dictionary? zona adherens explanation free. What is zona adherens? Meaning of zona adherens medical term. What does zona adherens mean?
Background: - Protein S-glutathionylation (Pr-SSG) is a prevalent form of oxidative modification of reactive cysteines and serves as an important mode of redox signaling. Vascular redox dysregulation and impaired barrier function have long been recognized as early vascular alterations in diabetes, a major risk factor for atherosclerotic cardiovascular diseases, but the mechanistic link of Pr-SSG to the metabolic stress-induced endothelial cell (EC) hyper-permeability is not established and being investigated in the present study.. Methods and Results: - elevated Pr-SSG was observed in ECs isolated from patients with type-2 diabetes and atherosclerotic lesions of ApoE deficient (ApoE-/-) mice, concurring with a decrease in glutaredoxin-1 (Glrx-1), a specific deglutathionylation enzyme. Exposure of human aortic ECs to diabetic conditions increased the formation of Pr-SSG and permeability that was associated with the disassembly of cell adherens junctions and cortical actin structures, all of which ...
Ukropec, Jon A., "Fluid shear stress-induced reorganization of adherens junctions in human endothelial cells" (1999). Theses. 24 ...
Haidari, M. et al. (2014). Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β-dependent vascular endothelial cadherin tyrosine phosphorylation. Cardiovasc Diabetol. 13:112.. Ackerman, W. et al. (2008). Nuclear Factor-kappa B regulates inducible prostaglandin E synthase expression in human amnion mesenchymal cells. Biol. Reprod. 78:68-76. ...
The function of connective tissues depends on the organisation of their collagen fibres, arranged in parallel fibres, in parallel sheets (lamellae; annulus fibrosus, cornea, bone), or with more complex or random, orientation (cartilage, dermis, loose connective tissue).. My research is on roles of the cytoskeleton and cell-cell interactions in control of secretion and orientation of the extracellular matrix in fibrous connective tissues.. In tendons, longitudinal rows of fibroblasts are embedded between parallel collagen fibre bundles. Along a row, cells are connected by gap junctions made of connexins 43 and 32, and by adherens junctions. The adherens junctions link short lengths of actin stress fibres end to end from cell to cell along the cell row.. Gap junctions modulate cell response to load: antisense downregulation of of connexin 43 enhances, and connexin 32 depresses, matrix secretion. Adherens junction and stress fibre components are upregulated by load suggesting that cells may bind ...
Although many organ functions rely on epithelial tubes with correct dimensions, mechanisms underlying tube size control are poorly understood. We analyse the cellular mechanism of tracheal tube elongation in Drosophila, and describe an essential role of the conserved tyrosine kinase Src42A in this process. We show that Src42A is required for polarized cell shape changes and cell rearrangements that mediate tube elongation. In contrast, diametric expansion is controlled by apical secretion independently of Src42A. Constitutive activation of Src42A induces axial cell stretching and tracheal overelongation, indicating that Src42A acts instructively in this process. We propose that Src42A-dependent recycling of E-Cadherin at adherens junctions is limiting for cell shape changes and rearrangements in the axial dimension of the tube. Thus, we define distinct cellular processes that independently control axial and diametric expansion of a cylindrical epithelium in a developing organ. Whereas ...
Vasioukhin V., Bowers E., Bauer C., Degenstein L., Fuchs E.. We have generated an epidermis-specific desmoplakin (DP) mouse knockout, and show that epidermal integrity requires DP; mechanical stresses to DP-null skin cause intercellular separations. The number of epidermal desmosomes in DP-null skin is similar to wild type (WT), but they lack keratin filaments, which compromise their function. DP-null keratinocytes have few desmosomes in vitro, and are unable to undergo actin reorganization and membrane sealing during epithelial sheet formation. Adherens junctions are also reduced. In vitro, DP transgene expression rescues these defects. DP is therefore required for assembly of functional desmosomes, maintaining cytoskeletal architecture and reinforcing membrane attachments essential for stable intercellular adhesion.. Nat. Cell Biol. 3:1076-1085(2001) [PubMed] [Europe PMC] ...
Xin actin-binding repeat-containing protein 2 is a protein that in humans is encoded by the XIRP2 gene. GRCh38: Ensembl release 89: ENSG00000163092 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000027022 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". Huang HT, Brand OM, Mathew M, Ignatiou C, Ewen EP, McCalmon SA, Naya FJ (Dec 2006). "Myomaxin is a novel transcriptional target of MEF2A that encodes a Xin-related alpha-actinin-interacting protein". J Biol Chem. 281 (51): 39370-9. doi:10.1074/jbc.M603244200. PMID 17046827. Sinn HW, Balsamo J, Lilien J, Lin JJ (Aug 2002). "Localization of the novel Xin protein to the adherens junction complex in cardiac and skeletal muscle during development". Dev Dyn. 225 (1): 1-13. doi:10.1002/dvdy.10131. PMID 12203715. Pacholsky D, Vakeel P, Himmel M, Lowe T, Stradal T, Rottner K, Furst DO, van der Ven PF (Oct 2004). "Xin repeats define a novel actin-binding motif". J Cell Sci. 117 (Pt 22): 5257-68. doi:10.1242/jcs.01406. ...
E-cadherin is a tumor suppressor protein that plays a crucial role in cell-cell adherens junction and tissue architecture and it is hypothesized to participate in carcinogenesis. It has been shown that a polymorphism in the upstream of the transcription start site of the CDH1 gene affects E-cadherin transcriptional regulation and seems to be associated with a variety of cancers. For the first time, we investigated the association of the rs16260 in the 5-untranslated region of the CDH1 gene with gastric cancer in Iranian population. Seventy- eight patients with gastric cancer and 72 healthy individuals were included and genotyped for this SNP using the PCR-RFLP method. Our results showed that the frequency of the AA genotype in gastric cancer patients (16 of 78, 20.5%) was higher than healthy individuals (9 of 72, 12.5%), the frequency of the A allele in the patients group was higher than controls (OR=1.231, 95% CI= 0.772-1.962, p-value= 0.383), but statistical analysis revealed the absence of
apical plasma membrane, cell-cell adherens junction, focal adhesion, actinin binding, protein C-terminus binding, ubiquitin-protein transferase activity, cell-cell adhesion
KAI1 (CD82) belongs to the transmembrane 4 superfamily in which members have inhibitory effects on tumor cell motility and metastasis. During reverse transcription-PCR analysis, we found a splice variant of KAI1 (spliced-KAI1) in which exon 7 was deleted. This exon encodes the 28 amino acids that span from the distal part of the second extracellular loop to the proximal part of the fourth transmembrane region. Expression of spliced-KAI1 was observed in metastatic tissues of gastric cancer patients with poor prognosis after operation. Genomic DNA analysis revealed that this variant was derived from the alternative splicing of exon 7. Immunoprecipitation showed that the interaction of spliced-KAI1 with integrin α3β1 was weaker than that of wild-type KAI1. Wild-type KAI1, but not spliced-KAI1, colocalized with E-cadherin, an adherens junction protein. Also, mouse colon adenocarcinoma cells stably expressing spliced-KAI1 (CT-26/spliced-KAI1) showed increased in vivo tumorigenicity, as well as ...
LOSS OF DELTA-CATENIN, A NEURONAL ADHERENS JUNCTION PROTEIN INTERACTING WITH PRESENILIN-1, LEADS TO SEVERE IMPAIRMENTS IN LEARNING AND SYNAPTIC PLASTICITY, AND MAY UNDERLIE THE MENTAL RETARDATION IN CRI-DU-CHAT SYNDROME.. A040.14. Poster 46 - Sun 11/07, 16:00 - Hall ...
To understand tissue morphogenesis and disease pathogenesis, ultimately we must understand what happens at the cellular and molecular levels. To do this, we use a number of techniques. To identify new protein-protein interactions important for establishing the machinery through which junctions carry out structural and signaling functions, we use in vitro biochemistry and a variety of protein interaction screens, including recently emerging Bio-ID proteomic approaches that allow for mapping nearest neighbors in cells and tissues in situ. How these protein interactions are regulated by post-translational modifications, including phosphorylation and protein methylation is also being uncovered through the use of mass spectrometry approaches.. To look at the importance of these protein interactions in cells, state-of-the-art optical imaging techniques are being employed. Fluorescently-tagged wild type and mutant desmosome and adherens junction molecules are tracked during intercellular junction ...
Disassembly of CAJs and abrogation of cadherin‐mediated cell-cell adhesion is involved in changes of cell state including differentiation, apoptosis and tumor metastasis. For example, induction of apoptotic cell death or Ca2+ imbalance involves cleavage of cadherins and disassembly of CAJs (Herren et al., 1998; Ito et al., 1999; Vallorosi et al., 2000; Steinhusen et al., 2001). Furthermore, in the case of metastasis of epithelia tumors, inhibition of E‐cadherin‐mediated cell-cell adhesion is promoted by cleavage and secretion of extracytoplasmic E‐cadherin by MMPs (Lochter et al., 1997; Christofori and Semb, 1999; Noe et al., 2001). Although in some cell cultures PS1 was found mainly in the ER-Golgi system (De Strooper et al., 1997; Cupers et al., 2001), in cell cultures with extensive cell-cell contacts and in tissues PS1 concentrates mainly at the plasma membrane (Georgakopoulos et al., 1999; Nowotny et al., 2000; Xia et al., 2001) and, in the brain, this protein concentrates at ...
An epithelial tissue is a sheet of cells that acts as a barrier, separating, for instance, the outside and the inside of a multicellular organism. Its biological function relies in part on the formation of a network of adherens junction belts, connected to the acto-myosin cytoskeleton, where cells adhere to each other [1], and which transmits mechanical information over several cell diameters [1-3]. A key issue is to understand and model the role of tissue mechanics (forces, displacements and their time evolution) in the coordinated changes of cell shape and position that determine morphogenetic flows at the tissue level [1,4,5].. Several models describe tissues using continuum mechanics [3,6-12]. One precondition is the existence of a mesoscopic scale defining a domain over which averages of cell properties are well defined [6,13]. This description further relies on the assumption that the tissue mechanical state can be quantified, at the same mesoscopic scale, by two variables [6]: the stress ...
Mouse Monoclonal Anti-E-Cadherin Antibody (67A4) [FITC]. Epithelial Cell Marker, Adherens Junctions Marker. Validated: Flow. Tested Reactivity: Human. 100% Guaranteed.
D. Leckband and Sivasankar, S., "Biophysics of cadherin adhesion", in Adherens junctions: from molecular mechanisms to tissue development and disease, Springer Netherlands, 2012, pp. 63-88. ...
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Karakesisoglou, I., Yang, Y. M. & Fuchs, E. (2000). An epidermal plakin that integrates actin and microtubule networks at cellular junctions. Journal Of Cell Biology 149(1): 195-208. ...
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Gap junctions are intercellular channels made of connexins (Cxs) that allow direct communication between adjacent cells. Modulation of Cxs has been associated with abnormal development and function of the mammary gland and breast cancer. However, the mechanisms underlying their expression during normal mammary gland are not yet known. Cxs interact with components of tight and adherens junctions. Thus, we hypothesized that the expression levels of Cxs vary during mammary gland development and are regulated through stage-dependent interactions with members of the tight and adherens junctions. Our specific objectives were to: 1) determine the expression of Cxs and tight and adherens junction proteins throughout development and 2) characterize Cxs interactions with components of tight and adherens junctions. Murine mammary glands were sampled at various developmental stages (pre-pubescent to post-weaning). RT-qPCR and western-blot analyses demonstrated differential expression patterns for all gap ...
TY - JOUR. T1 - Glutamine supplementation attenuates ethanol-induced disruption of apical junctional complexes in colonic epithelium and ameliorates gut barrier dysfunction and fatty liver in mice. AU - Chaudhry, Kamaljit K.. AU - Shukla, Pradeep Kumar. AU - Mir, Hina. AU - Manda, Bhargavi. AU - Gangwar, Ruchika. AU - Yadav, Nikki. AU - McMullen, Megan. AU - Nagy, Laura E.. AU - Rao, Radhakrishna. PY - 2016/1/1. Y1 - 2016/1/1. N2 - Previous in vitro studies showed that glutamine (Gln) prevents acetaldehyde-induced disruption of tight junctions and adherens junctions in Caco-2 cell monolayers and human colonic mucosa. In the present study, we evaluated the effect of Gln supplementation on ethanol-induced gut barrier dysfunction and liver injury in mice in vivo. Ethanol feeding caused a significant increase in inulin permeability in distal colon. Elevated permeability was associated with a redistribution of tight junction and adherens junction proteins and depletion of detergent-insoluble ...
Background and Objective: Impairment of the regulation of tissue fluid homeostasis and migration of blood cells across the endothelial barrier are crucial factors in the pathogenesis of acute lung injury (ALI). Thus, a goal for treatment of ALI is to target the pathways that lead to profound dysregulation of the restrictive endothelial barrier, and thereby restore lung microvascular endothelial barrier function and inhibit protein-rich tissue fluid accumulation. Here we test the hypothesis that epigenetic modifiers TSA (Trichostatin-A, a HDAC inhibitor) and Aza (5-aza-2-deoxycytidine, a DNA methyl transferase inhibitor) together inhibit the LPS/thrombin induced eNOS/RhoA signaling and restore AJ integrity and diminished endothelial hyperpermeability.. Methods and Results: The signaling, AJ integrity and endothelial permeability were assessed by RT-PCR and western blot analysis; transendothelial resistance (TER) and lung endothelial permeability were measured by capillary filtration coefficient ...